Paradoxical kinesia in parkinsonism is not caused by dopamine release. Studies in an animal model.

Rats become akinetic after large dopamine-depleting brain lesions, yet they show an activation-induced restoration of motor function. In this study, rats were given intraventricular injections of the neurotoxin 6-hydroxydopamine to permanently reduce the dopamine content of the corpus striatum by 98%. Although the rats were akinetic in their home cages, they swam effectively when placed in deep water and escaped from a shallow floating ice bath. These behaviors were not abolished by pretreating the animals with the dopamine antagonists haloperidol and SCH-23390. In contrast, haloperidol completely blocked the brain-damaged animals' behavioral responses to amphetamine. These results suggest that the paradoxical kinesia of dopamine-depleted rats is not a consequence of dopamine release from residual dopaminergic fibers.

[1]  E. Abercrombie,et al.  Differential Effect of Stress on In Vivo Dopamine Release in Striatum, Nucleus Accumbens, and Medial Frontal Cortex , 1989, Journal of neurochemistry.

[2]  B. Jacobs,et al.  Lack of response of serotonergic neurons in the dorsal raphe nucleus of freely moving cats to stressful stimuli , 1988, Experimental Neurology.

[3]  Theodore W. Berger,et al.  Interactions between dopamine and amino acid-induced excitation and inhibition in the striatum , 1986, Brain Research.

[4]  J. Liebman,et al.  SCH 23390 dissociated from conventional neuroleptics in apomorphine climbing and primate acute dyskinesia models. , 1985, Life sciences.

[5]  J. Hyttel Functional evidence for selective dopamine D-1 receptor blockade by SCH 23390 , 1984, Neuropharmacology.

[6]  M. Zigmond,et al.  Environmental stimuli but not homeostatic challenges produce apparent increases in dopaminergic activity in the striatum: An analysis by in vivo voltammetry , 1983, Brain Research.

[7]  A. Barnett,et al.  SCH 23390, a potential benzazepine antipsychotic with unique interactions on dopaminergic systems. , 1983, The Journal of pharmacology and experimental therapeutics.

[8]  J. Barchas,et al.  Epinephrine, norepinephrine, dopamine and serotonin: Differential effects of acute and chronic stress on regional brain amines , 1982, Brain Research.

[9]  J. Hyttel Similarities between the binding of 3H-piflutixol and 3H-flupentixol to rat striatal dopamine receptors in vitro. , 1981, Life sciences.

[10]  J. Barchas,et al.  Simultaneous determination of catecholamines and unconjugated 3,4-dihydroxyphenylacetic acid in brain tissue by ion-pairing reverse-phase high-performance liquid chromatography with electrochemical detection. , 1980, Analytical biochemistry.

[11]  Louis A. Chiodo,et al.  Sensory stimuli alter discharge rate of dopamine (DA) neurons: evidence for two functional types of DA cells in the substantia nigra , 1980, Brain Research.

[12]  L. Chiodo,et al.  Reciprocal influences of activating and immobilizing stimuli on the activity of nigrostriatal dopamine neurons , 1979, Brain Research.

[13]  Laurent Descarries,et al.  Modulatory role for biogenic amines in the cerebral cortex. Microiontophoretic studies , 1979, Brain Research.

[14]  R. George,et al.  Subcellular localization of dopamine-sensitive adenylate cyclase and dopamine receptor binding activities. , 1978, Life sciences.

[15]  C. H. Vanderwolf,et al.  Behavior of the rat after removal of the neocortex and hippocampal formation. , 1978, Journal of comparative and physiological psychology.

[16]  A. Oke,et al.  Liquid chromatographic analysis of catecholamines routine assay for regional brain mapping. , 1976, Life sciences.

[17]  S. Antelman,et al.  Interactive effects of brain catecholamines and variations in sexual and non-sexual arousal on copulatory behavior of male rats , 1976, Brain Research.

[18]  E. Stricker,et al.  Activation-induced restoration of sensorimotor functions in rats with dopamine-depleting brain lesions. , 1976, Journal of comparative and physiological psychology.

[19]  E. Stricker Drinking by rats after lateral hypothalamic lesions: a new look at the lateral hypothalamic syndrome. , 1976, Journal of comparative and physiological psychology.

[20]  P. Teitelbaum,et al.  Somnolence, akinesia, and sensory activation of motivated behavior in the lateral hypothalamic syndrome. , 1975, Proceedings of the National Academy of Sciences of the United States of America.

[21]  P. Teitelbaum,et al.  Nigrostriatal bundle damage and the lateral hypothalamic syndrome. , 1974, Journal of comparative and physiological psychology.

[22]  P. Teitelbaum,et al.  Dissociation between learning and remembering in rats with lesions in the lateral hypothalamus. , 1974, Journal of comparative and physiological psychology.

[23]  T. Robinson,et al.  Effects of posterior hypothalamic lesions on voluntary behavior and hippocampal electroencephalograms in the rat. , 1974, Journal of comparative and physiological psychology.

[24]  M. Zigmond,et al.  Recovery of Feeding and Drinking by Rats after Intraventricular 6-Hydroxydopamine or Lateral Hypothalamic Lesions , 1973, Science.

[25]  M. Salas,et al.  Hormonal Effects on Ontogeny of Swimming Ability in the Rat: Assessment of Central Nervous System Development , 1970, Science.

[26]  A. Anton,et al.  A study of the factors affecting the aluminum oxide-trihydroxyindole procedure for the analysis of catecholamines. , 1962, The Journal of pharmacology and experimental therapeutics.

[27]  G. Mogenson,et al.  Limbic-motor integration , 1987 .

[28]  D. Sibley,et al.  The classification of dopamine receptors: relationship to radioligand binding. , 1983, Annual review of neuroscience.

[29]  H. Lal,et al.  Behavioral Actions of Neuroleptics , 1978 .

[30]  R. Schwab,et al.  Effects of mood, motivation, stress and alertness on the performance in Parkinson's disease. , 1965, Psychiatria et neurologia.